We are analyzing https://link.springer.com/article/10.1007/s00125-015-3651-3.

Title:
Contribution of brown adipose tissue activity to the control of energy balance by GLP-1 receptor signalling in mice | Diabetologia
Description:
Aims/hypothesis We assessed the contribution of glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) signalling to thermogenesis induced by high-fat diet (HFD) consumption. Furthermore, we determined whether brown adipose tissue (BAT) activity contributes to weight loss induced by chronic subcutaneous treatment with the GLP-1R agonist, liraglutide, in a model of diet-induced obesity. Methods Metabolic phenotyping was performed using indirect calorimetry in wild-type (WT) and Glp1r-knockout (KO) mice during chow and HFD feeding at room temperature and at thermoneutrality. In a separate study, we investigated the contribution of BAT thermogenic capacity to the weight lowering effect induced by GLP-1 mimetics by administering liraglutide (10 or 30 nmol kg−1 day−1 s.c.) to diet-induced obese (DIO) mice for 6 or 4 weeks, respectively. In both studies, animals were subjected to a noradrenaline (norepinephrine)-stimulated oxygen consumption V ⋅ O 2 $$ \left(\overset{\cdot }{V}{\mathrm{O}}_2\right) $$ test. Results At thermoneutrality, HFD-fed Glp1r-KO mice had similar energy expenditure (EE) compared with HFD-fed WT controls. However, HFD-fed Glp1r-KO mice exhibited relatively less EE when housed at a cooler standard room temperature, and had relatively lower V ⋅ O 2 $$ \overset{\cdot }{V}{\mathrm{O}}_2 $$ in response to a noradrenaline challenge, which is consistent with impaired BAT thermogenic capacity. In contrast to the loss of function model, chronic peripheral liraglutide treatment did not increase BAT activity as determined by noradrenaline-stimulated V ⋅ O 2 $$ \overset{\cdot }{V}{\mathrm{O}}_2 $$ and BAT gene expression. Conclusions/interpretation These data suggest that although endogenous GLP-1R signalling contributes to increased BAT thermogenesis, this mechanism does not play a significant role in the food intake-independent body weight lowering effect of the GLP-1 mimetic liraglutide in DIO mice.
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Keywords {🔍}

mice, bat, oversetcdot, vmathrmo, liraglutide, pubmed, article, glpr, fig, thermogenesis, nmol, glprko, activity, google, scholar, animals, compared, significantly, energy, cas, signalling, lower, day, hfdfed, vehiclepf, glp, bars, data, adipose, tissue, brown, treatment, similar, food, loss, central, intake, weight, noradrenaline, obesity, hfd, temperature, expression, anova, contribution, effect, gene, role, white, control,

Topics {✒️}

central glp-1r signalling hfd-fed glp1r-ko mice cd-fed glp1r-ko animals full size image endogenous glp-1r signalling glp-1r signalling plays 30 nmol kg−1 day−1 liraglutide-treated diego perez-tilve glp-1r-mediated activation 30 nmol kg−1 day−1 reduced feeding vehicle-treated pair-fed group 10 nmol kg−1 day−1 liraglutide study glp1r-ko mice preserved abolishes diet-induced thermogenesis glp1r-ko mice fed hfd-fed glp1r-ko glp1r-ko hfd-fed food intake-independent reduction gene-specific taqman assays glp-1/glp-1r signaling male c57bl/6j mice lean chow-fed mice central nervous system glp1r-ko mice compared chow-fed conditions remains age-matched wild-type brown adipose tissue brown adipose tissue glp1r-ko mice maintained 30 nmol kg−1 day−1 study 30 nmol kg−1 day−1 liraglutide vehicle-pair-fed mice high-fat diet glp-1r agonist glp-1rs increases endogenous glp-1r recent evidence revealing mice article published vehicle-pf treated mice liraglutide-treated mice compared 30 nmol kg−1 liraglutide study hfd-fed wt controls hfd-fed wt compared high-sucrose diet glp-1 receptor signalling kmh receives funding glp-1r signalling weight lowering effect privacy choices/manage cookies bw lowering effects

Questions {❓}

Tong J, Sandoval DA (2011) Is the GLP-1 system a viable therapeutic target for weight reduction?

Schema {🗺️}

WebPage:
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         headline:Contribution of brown adipose tissue activity to the control of energy balance by GLP-1 receptor signalling in mice
         description:We assessed the contribution of glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) signalling to thermogenesis induced by high-fat diet (HFD) consumption. Furthermore, we determined whether brown adipose tissue (BAT) activity contributes to weight loss induced by chronic subcutaneous treatment with the GLP-1R agonist, liraglutide, in a model of diet-induced obesity. Metabolic phenotyping was performed using indirect calorimetry in wild-type (WT) and Glp1r-knockout (KO) mice during chow and HFD feeding at room temperature and at thermoneutrality. In a separate study, we investigated the contribution of BAT thermogenic capacity to the weight lowering effect induced by GLP-1 mimetics by administering liraglutide (10 or 30 nmol kg−1 day−1 s.c.) to diet-induced obese (DIO) mice for 6 or 4 weeks, respectively. In both studies, animals were subjected to a noradrenaline (norepinephrine)-stimulated oxygen consumption $$ \left(\overset{\cdot }{V}{\mathrm{O}}_2\right) $$ test. At thermoneutrality, HFD-fed Glp1r-KO mice had similar energy expenditure (EE) compared with HFD-fed WT controls. However, HFD-fed Glp1r-KO mice exhibited relatively less EE when housed at a cooler standard room temperature, and had relatively lower $$ \overset{\cdot }{V}{\mathrm{O}}_2 $$ in response to a noradrenaline challenge, which is consistent with impaired BAT thermogenic capacity. In contrast to the loss of function model, chronic peripheral liraglutide treatment did not increase BAT activity as determined by noradrenaline-stimulated $$ \overset{\cdot }{V}{\mathrm{O}}_2 $$ and BAT gene expression. These data suggest that although endogenous GLP-1R signalling contributes to increased BAT thermogenesis, this mechanism does not play a significant role in the food intake-independent body weight lowering effect of the GLP-1 mimetic liraglutide in DIO mice.
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            Liraglutide
            Internal Medicine
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            Human Physiology
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      headline:Contribution of brown adipose tissue activity to the control of energy balance by GLP-1 receptor signalling in mice
      description:We assessed the contribution of glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) signalling to thermogenesis induced by high-fat diet (HFD) consumption. Furthermore, we determined whether brown adipose tissue (BAT) activity contributes to weight loss induced by chronic subcutaneous treatment with the GLP-1R agonist, liraglutide, in a model of diet-induced obesity. Metabolic phenotyping was performed using indirect calorimetry in wild-type (WT) and Glp1r-knockout (KO) mice during chow and HFD feeding at room temperature and at thermoneutrality. In a separate study, we investigated the contribution of BAT thermogenic capacity to the weight lowering effect induced by GLP-1 mimetics by administering liraglutide (10 or 30 nmol kg−1 day−1 s.c.) to diet-induced obese (DIO) mice for 6 or 4 weeks, respectively. In both studies, animals were subjected to a noradrenaline (norepinephrine)-stimulated oxygen consumption $$ \left(\overset{\cdot }{V}{\mathrm{O}}_2\right) $$ test. At thermoneutrality, HFD-fed Glp1r-KO mice had similar energy expenditure (EE) compared with HFD-fed WT controls. However, HFD-fed Glp1r-KO mice exhibited relatively less EE when housed at a cooler standard room temperature, and had relatively lower $$ \overset{\cdot }{V}{\mathrm{O}}_2 $$ in response to a noradrenaline challenge, which is consistent with impaired BAT thermogenic capacity. In contrast to the loss of function model, chronic peripheral liraglutide treatment did not increase BAT activity as determined by noradrenaline-stimulated $$ \overset{\cdot }{V}{\mathrm{O}}_2 $$ and BAT gene expression. These data suggest that although endogenous GLP-1R signalling contributes to increased BAT thermogenesis, this mechanism does not play a significant role in the food intake-independent body weight lowering effect of the GLP-1 mimetic liraglutide in DIO mice.
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         GLP-1
         High-fat diet
         Liraglutide
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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               type:PostalAddress
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      name:Department of Chemistry, Indiana University, Bloomington, USA
      name:Metabolic Diseases Institute, Department of Medicine/Internal Medicine, University of Cincinnati, Cincinnati, USA

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